Cell Growth: Cancer

Question 1

G1 Cdk

Answer 1

Cdk that promotes cell division
Drives G1 / S Cdk to proceed through START
Promoted by mitogens
Called: Cyclin D / cdk4 and Cyclin D / cdk6

Question 2

Mitogens

Answer 2

Can be peptides or lipids
Peptides: PDGF, EGF, FGF
Lipids: LPA, S1P

Question 3

Role of G1 Cdk (Cyclin D / Cdk 4 & Cyclin D / Cdk 6)

Answer 3

G1 Cdk phosphorylates Rb protein
Phosphorylated Rb protein releases E2F in the nucleus
E2F can then transcribe genes coding for G1/S Cdk to go through START

Question 4

How do mitogens activate G1 Cdk?

Answer 4

Signal through Ras and PI3K
Ras leads to Cyclin D expression
PI3K activates PKB (AKT), which inactivates transport of G1-Cdk (cyclin D / Cdc 4) out of the nucleus

Question 5

p27

Answer 5

When bound to G1-Cdk active
When bound to G1/S Cdk inactive
Helps ensure G1-Cdk has produced enough products before going through START

Question 6

Guardian of the Genome

Answer 6

p53
Transcription factor that promotes transcription of cell cycle inhibitiors i.e. CKI p21
p21 binds to G1 -cdk and does not allow for progression through START

Question 7

T of F p53 is short lived?

Answer 7

True p53 is associated with Mdm 2 which is a ubiquitination ligase

Question 8

Too much Mitogens signals?

Answer 8

Alternative pathway through MAPK that inhibits MDM2 and allows p53 to inhibit G1 -Cdk expression via p21 and stimulate apoptosis

Question 9

Tumor Cells/ Tissue Have

Answer 9

Loss of mitogen dependence
Loss of contact inhibition
Loss of anchorage dependence
Cell shape changes due to changes in adhesion and motility

Question 10

Oncogenes act

Answer 10

Dominantly

Only need to mutate one gene

Question 11

Tumor Suprressor Genes act

Answer 11

Recessively

Need to loose both functional genes